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Vol. 13, Issue 9, 3218-3234, September 2002
and¶
*Cystic Fibrosis/Pulmonary Research and Treatment Center, and the
Departments of Epithelial tight junctions (TJs) provide an important route for
passive electrolyte transport across airway epithelium and provide a
barrier to the migration of toxic materials from the lumen to the
interstitium. The possibility that TJ function may be perturbed by
airway inflammation originated from studies reporting (1) increased
levels of the proinflammatory cytokines interleukin-8 (IL-8), tumor
necrosis factor Medicine, Pharmacology,
§Pediatrics, and Cell and Developmental
Biology, The University of North Carolina at Chapel Hill, Chapel Hill,
North Carolina 27599
(TNF-), interferon 
(IFN-), and IL-1
in
airway epithelia and secretions from cystic fibrosis (CF) patients and
(2) abnormal TJ strands of CF airways as revealed by freeze-fracture
electron microscopy. We measured the effects of cytokine exposure of CF
and non-CF well-differentiated primary human airway epithelial cells on
TJ properties, including transepithelial resistance, paracellular
permeability to hydrophilic solutes, and the TJ proteins occludin,
claudin-1, claudin-4, junctional adhesion molecule, and ZO-1. We found
that whereas IL-1 treatment led to alterations in TJ ion
selectivity, combined treatment of TNF- and IFN- induced profound
effects on TJ barrier function, which could be blocked by inhibitors of
protein kinase C. CF bronchi in vivo exhibited the same pattern of
expression of TJ-associated proteins as cultures exposed in vitro to
prolonged exposure to TNF- and IFN-. These data indicate that the
TJ of airway epithelia exposed to chronic inflammation may exhibit
parallel changes in the barrier function to both solutes and ions.
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